Pharmacological inhibition of S100A9 prolongs survival in adoptive transfer Eμ-TCL1 mice. Splenocytes from Eμ-TCL1 mice were transferred via TVI into C57BL/6 mice, and PaQ and TasQ were administered at 25 mg/kg in drinking water for 4 weeks. (A) Tumor burden assessment in the PB using FC. (B) Representative picture of the 3 mice groups after 4 weeks of treatment. (C-D) Spleen weight and infiltration after 4 weeks of treatment. (E) Mice treated with PaQ or TasQ show longer survival than the control group. (F) Volcano plot showing differential gene expression in B cells from PaQ vs vehicle using NanoString PanCancer Immune Profiling panel. (G) Downregulated genes in PaQ-treated B cells relative to B cells from vehicle-recipient mice, belonging to the TNF-α signaling via NF-κB from the MSigDB Hallmark genes. ∗∗∗∗P < .0001; ∗∗∗P < .001; ∗∗P < .005; ∗P < .05. ns, not significant.
Figure 5.

Pharmacological inhibition of S100A9 prolongs survival in adoptive transfer Eμ-TCL1 mice. Splenocytes from Eμ-TCL1 mice were transferred via TVI into C57BL/6 mice, and PaQ and TasQ were administered at 25 mg/kg in drinking water for 4 weeks. (A) Tumor burden assessment in the PB using FC. (B) Representative picture of the 3 mice groups after 4 weeks of treatment. (C-D) Spleen weight and infiltration after 4 weeks of treatment. (E) Mice treated with PaQ or TasQ show longer survival than the control group. (F) Volcano plot showing differential gene expression in B cells from PaQ vs vehicle using NanoString PanCancer Immune Profiling panel. (G) Downregulated genes in PaQ-treated B cells relative to B cells from vehicle-recipient mice, belonging to the TNF-α signaling via NF-κB from the MSigDB Hallmark genes. ∗∗∗∗P < .0001; ∗∗∗P < .001; ∗∗P < .005; ∗P < .05. ns, not significant.

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